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From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. The Notch signalling is a major regulator of cardiovascular function and it is also implicated in several biological processes mediating viral infections. In this report we discuss the possibility to target Notch signalling to prevent SARS-CoV-2 infection and interfere with the progression of COVID-19- associated heart and lungs disease.

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Gene expressions in the myocardium have been shown to vary between different causes of death, which can be utilized in the recognition of varied processes. Our previous work with a limited number of cases showed a high messenger ribonucleic acid expression of the transcript variant alt-a of cyclin dependent kinase inhibitor p21 (p21 alt-a) in chronic cardiac ischemia deaths and a low expression in hypothermia deaths and acute myocardial ischemia deaths. In present work, p21 alt-a expression in the myocardium of human cadavers was calculated using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as reference gene. In this collection of 143 samples, the p21 alt-a expression was significantly lower in hypothermia than in chronic cardiac ischemic heart disease with (Pâ

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The pulse wave transit time (PWTT) is easily measured as the time from the R wave of an electrocardiogram to the arrival of the pulse wave measured by an oxygen saturation monitor at the earlobe. We investigated whether the change of PWTT during exercise testing reflects cardiopulmonary function. Eighty-nine cardiac patients who underwent cardiopulmonary exercise testing (CPX) were enrolled. We analyzed the change of PWTT during exercise and the relationship between the shortening of the PWTT and CPX parameters. PWTT was significantly shortened from rest to peak exercise (204.6 ± 33.6 vs. 145.6 ± 26.4 msec, p < 0.001) in all of the subjects. The patients with heart failure had significantly higher PWTT at peak exercise than the patients without heart failure (152.7 ± 27.1 vs. 140.4 ± 24.8 msec, p = 0.031). The shortening of PWTT from rest to peak exercise showed significant positive correlations with the peak O2 uptake (VO2) (r = 0.56, p < 0.001), anaerobic threshold (r = 0.40, p = 0.016), and % increase of systolic blood pressure during exercise (r = 0.75, p < 0.001), and a negative correlation with the slope of the increase in ventilation versus the increase in CO2 output (VE-VCO2 slope) (r = - 0.42, p = 0.010) in the patients with heart failure. PWTT was shortened during exercise as the exercise intensity increased. In the patients with heart failure, the shortening of PWTT from rest to peak exercise was smaller in those with lower exercise capacity and those with higher VE-VCO2 slope, an established index known to reflect the severity of heart failure.

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The plasma membrane is an important cellular organelle that is often overlooked in terms of a primary factor in regulating physiology and pathophysiology. There is emerging evidence to suggest that the plasma membrane serves a greater purpose than a simple barrier or transporter of ions. New paradigms suggest that the membrane serves as a critical bridge to connect extracellular to intracellular communication particularly to regulate energy and metabolism by forming physical and biochemical associations with intracellular organelles. This review will focus on the relationship of a particular membrane microdomain - caveolae - with mitochondria and the particular implication of this to physiology and pathophysiology.

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The sarco-endoplasmic reticulum (SR/ER) plays an important role in the development and progression of many heart diseases. However, many aspects of its structural organization remain largely unknown, particularly in cells with a highly differentiated SR/ER network. Here, we report a cardiac enriched, SR/ER membrane protein, REEP5 that is centrally involved in regulating SR/ER organization and cellular stress responses in cardiac myocytes. In vitro REEP5 depletion in mouse cardiac myocytes results in SR/ER membrane destabilization and luminal vacuolization along with decreased myocyte contractility and disrupted Ca2+ cycling. Further, in vivo CRISPR/Cas9-mediated REEP5 loss-of-function zebrafish mutants show sensitized cardiac dysfunction upon short-term verapamil treatment. Additionally, in vivo adeno-associated viral (AAV9)-induced REEP5 depletion in the mouse demonstrates cardiac dysfunction. These results demonstrate the critical role of REEP5 in SR/ER organization and function as well as normal heart function and development.

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BACKGROUND: Type 1 diabetes mellitus (T1DM) in children and adolescents is associated with significant cardiovascular morbidity and mortality. Early detection of vascular dysfunction is key to patient management yet current assessment techniques are invasive and not suitable for pediatric patient populations. A novel approach using isometric handgrip exercise during magnetic resonance imaging (IHE-MRI) has recently been developed to evaluate coronary endothelial function non-invasively in adults. This project aimed to assess endothelium-dependent coronary arterial response to IHE-MRI in children with T1DM and in age matched healthy controls. MATERIALS AND METHODS: Healthy volunteers and children with T1DM (>5 years) were recruited. IHE-MRI cross-sectional coronary artery area measurements were recorded at rest and under stress. Carotid intima media thickness (CIMT) and aortic pulse wave velocity (PWV) were assessed for comparison. Student's t-tests were used to compare results between groups. RESULTS AND DISCUSSION: Seven children with T1DM (3 female, median 14.8 years, mean 14.8 ± 1.9 years) and 16 healthy controls (7 female, median 14.8 years, mean 14.2 ± 2.4 years) participated. A significant increase in stress-induced cross-sectional coronary area was measured in controls (5.4 mm2 at rest to 6.39 mm2 under stress, 18.8 ± 10.7%, p = 0.0004). In contrast, mean area change in patients with T1DM was not significant (7.17 mm2 at rest to 7.59 mm2 under stress, 10.5% ± 28.1%, p = n.s.). There was no significant difference in the results for neither PWV nor CIMT between patients and controls, (5.3±1.5 m/s vs.4.8±0.7 m/s and 0.4±0.03mm vs.0.46 mm ± 0.03 respectively, both p = n.s.). CONCLUSIONS: Our pilot study demonstrates the feasibility of using a totally non-invasive IHE-MRI technique in children and adolescents with and without T1DM. Preliminary results suggest a blunted endothelium-dependent coronary vasomotor function in children with T1DM (>5 years). Better knowledge and new methodologies may improve surveillance and care for T1DM patients to reduce cardiovascular morbidity and mortality.

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The presence of hypertensive mediated organ damage is related to increased vascular risk and mortality and its prevention should be a therapeutic target and a surrogate marker of in/adequate blood pressure control. In old adult hypertensive patients the therapeutic target should be to prevent major cardiovascular events, but in young hypertensive subjects the focus should be pointed on preventing the development of hypertensive mediated organ damage, since most of the hard events are preceded by functional and structural tissues injury. Hypertension Guidelines of the European Society of Cardiology and European Society of Hypertension recognizes that some variables like electrocardiographic or echocardiographic left ventricle hypertrophy, chronic kidney disease or advance retinopathy, all considered as hypertensive mediated organ damage, may be modifiers of cardiovascular risk estimated by the SCORE system, and for that reason they should be screened in hypertensive patients. It is well known the problem of limited health systems financial resources in many low and even median income countries which precludes the possibilities of generalizing the search for hypertension mediated organ damage in all hypertensive patients. In these scenario the recommendation to perform a detailed screening should be critically evaluated. Some questions remained unanswered: the screening generalization of hypertensive mediated organ damage should modify the cardiovascular risk score of the patients, if its presence could modify the therapeutic approach, and as a consequence, if the treatment adjustment should prolong life expectancy and ameliorate the quality of life.

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Cardiac autonomic neuropathy (CAN) is an underdiagnosed cardiovascular complication associated with diabetes. NPs are in a pivotal position to screen patients for CAN. As the incidence of diabetes increases in an aging population, NPs can help prevent complications associated with diabetes and CAN.

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Evaluation of myocardial regional function is generally performed by visual "eyeballing" which is highly subjective. A robust quantifiable parameter of regional function is required to provide an objective, repeatable and comparable measure of myocardial performance. We aimed to evaluate the clinical utility of novel regional myocardial strain software from cardiac computed tomography (CT) datasets. 93 consecutive patients who had undergone retrospectively gated cardiac CT were evaluated by the software, which utilizes a finite element based tracking algorithm through the cardiac cycle. Circumferential (CS), longitudinal (LS) and radial (RS) strains were calculated for each of 16 myocardial segments and compared to a visual assessment, carried out by an experienced cardiologist on cine movies of standard "echo" views derived from the CT data. A subset of 37 cases was compared to speckle strain by echocardiography. The automated software performed successfully in 93/106 cases, with minimal human interaction. Peak CS, LS and RS all differentiated well between normal, hypokinetic and akinetic segments. Peak strains for akinetic segments were generally post-systolic, peaking at 50 ± 17% of the RR interval compared to 43 ± 9% for normokinetic segments. Using ROC analysis to test the ability to differentiate between normal and abnormal segments, the area under the curve was 0.84 ± 0.01 for CS, 0.80 ± 0.02 for RS and 0.68 ± 0.02 for LS. There was a moderate agreement with speckle strain. Automated 4D regional strain analysis of CT datasets shows a good correspondence to visual analysis and successfully differentiates between normal and abnormal segments, thus providing an objective quantifiable map of myocardial regional function.

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Impaired cardiovascular and autonomic function during treatment and during recovery from leukemia has been indicated. In this context, heart rate variability (HRV) is a non-invasive measure that describes the oscillations of the intervals between consecutive heart beats (RR intervals), influenced by the autonomic nervous system. We intend to review literature showing HRV changes in leukemia subjects. The articles selected in the current review were attained up to March 2018, and the search was limited to articles in English language, published in peer-reviewed journals, with both adult and child age samples. The articles were investigated in the five electronic databases: PubMed, Physiotherapy Evidence Database (PEDro), Cochrane Clinical Trials, Scientific Electronic Library Online (SciELO), and Excerpta Medica dataBASE (EMBASE). Towards the end of the research, 9 studies were included. Subjects undergoing treatment for leukemia have reduced HRV, signifying decreased vagal control of heart rate. The subjects that undertook leukemia treatment and their survivors experienced a reduction in HRV with subsequent recovery, but the recovery time is ill defined. HRV is reduced in leukemia subjects who progress to neuropathy secondary to chemotherapy, accompanied by cardiac dysfunction. We advocate the use of HRV to evaluate autonomic function and decide the treatment to prevent autonomic impairment in leukemia subjects.

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Sphingolipids are key signaling molecules involved in the regulation of cell physiology. These species are found in tissues and in circulation. Although they only constitute a small fraction in lipid composition of circulating lipoproteins, their concentration in plasma and distribution among plasma lipoproteins appears distorted under adverse cardiometabolic conditions such as diabetes mellitus. Sphingosine-1-phosphate (S1P), one of their main representatives, is involved in regulating cardiomyocyte homeostasis in different models of experimental cardiomyopathy. Cardiomyopathy is a common complication of diabetes mellitus and represents a main risk factor for heart failure. Notably, plasma concentration of S1P, particularly high-density lipoprotein (HDL)-bound S1P, may be decreased in patients with diabetes mellitus, and hence, inversely related to cardiac alterations. Despite this, little attention has been given to the circulating levels of either total S1P or HDL-bound S1P as potential biomarkers of diabetic cardiomyopathy. Thus, this review will focus on the potential role of HDL-bound S1P as a circulating biomarker in the diagnosis of main cardiometabolic complications frequently associated with systemic metabolic syndromes with impaired insulin signaling. Given the bioactive nature of these molecules, we also evaluated its potential of HDL-bound S1P-raising strategies for the treatment of cardiometabolic disease.

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Human-based modelling and simulations are becoming ubiquitous in biomedical science due to their ability to augment experimental and clinical investigations. Cardiac electrophysiology is one of the most advanced areas, with cardiac modelling and simulation being considered for virtual testing of pharmacological therapies and medical devices. Current models present inconsistencies with experimental data, which limit further progress. In this study, we present the design, development, calibration and independent validation of a human-based ventricular model (ToR-ORd) for simulations of electrophysiology and excitation-contraction coupling, from ionic to whole-organ dynamics, including the electrocardiogram. Validation based on substantial multiscale simulations supports the credibility of the ToR-ORd model under healthy and key disease conditions, as well as drug blockade. In addition, the process uncovers new theoretical insights into the biophysical properties of the L-type calcium current, which are critical for sodium and calcium dynamics. These insights enable the reformulation of L-type calcium current, as well as replacement of the hERG current model.

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OBJECTIVE: Pegylated liposomal doxorubicin (PLD) has similar reported clinical efficacy compared with conventional doxorubicin with less cardiotoxicity. The manufacturer of PLD advises that cardiac function should be evaluated with endomyocardial biopsy, echocardiography or multigated radionucleotide scan (MUGA) pre-treatment and during therapy. This study was designed to assess the necessity of pre-treatment cardiac evaluation in patients receiving PLD. METHODS: After IRB approval, a retrospective study of all women with gynecologic cancer who received PLD from 2006 to 2018 was performed. Demographic information, treatment records, cardiac risk factors, and cardiac surveillance testing were examined. Wilcoxon signed rank sum test and logistic regression were used to evaluate the association of cumulative PLD exposure with cardiotoxicity. RESULTS: A total of 235 patients received PLD for gynecologic cancer. Patients received a median of 3â¯cycles of PLD with a cumulative dosage of 237â¯mg over a median follow-up time of 24â¯months. Sixteen patients in the cohort (7%) had no cardiac surveillance at all. Of the remaining patients who underwent cardiac testing, 183 (84%) received MUGA scans and 36 (16%) had echocardiography. Of the 56 patients who had both pre- and post-treatment cardiac testing, there was no significant difference in median ejection fraction (pâ¯=â¯0.17). Three patients developed PLD-associated cardiac toxicity but only one patient had severe manifestations requiring discontinuation of PLD therapy. CONCLUSIONS: Routine cardiac testing before, during or after treatment with PLD may be unnecessary. Cardiac testing may be more appropriate for individual patients for whom the clinical suspicion of PLD-related cardiac toxicity is high.

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High blood pressure (BP) is becoming a growing health issue even in children and adolescents. Moreover, BP elevation in youth frequently translates into children and adult hypertension contributing to the development of cardiovascular disease. The detection of early markers of vascular damage, potentially leading to overt cardiovascular disease, is important for clinical decisions about if and how to treat hypertension and can be useful in monitoring the effectiveness of the treatment. The purpose of this review is to summarize the actual knowledge about subclinical organ damage (SOD) in hypertensive children and adolescents and its association with cardiovascular disease in children and young adults. Our focus is especially put on left ventricular mass, pulse wave velocity, carotid intima-media thickness and microalbuminuria. We also want to address the scientific evidence about possible regression of SOD and cardiovascular risk with the use of behavioural and specific anti-hypertensive therapy. Indications from current guidelines are critically discussed.

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Ghrelin, a growth hormone-releasing peptide first discovered in rat stomach in 1999, is a ligand for the growth hormone secretagogue receptor. It participates in the regulation of diverse processes, including energy balance and body weight maintenance, and appears to be beneficial for the treatment of cardiovascular diseases. In animal models of chronic heart failure, ghrelin improves cardiac function and remodeling; these findings have been recapitulated in human patients. In other animal models, ghrelin effectively diminishes pulmonary hypertension. Moreover, ghrelin administration early after myocardial infarction decreased the frequency of fatal arrhythmia and improved survival rate. In ghrelin-deficient mice, endogenous ghrelin protects against fatal arrhythmia and promotes remodeling after myocardial infarction. Although the mechanisms underlying the effects of ghrelin on the cardiovascular system have not been fully elucidated, its beneficial effects appear to be mediated through regulation of the autonomic nervous system. Ghrelin is a promising therapeutic agent for cardiac diseases.

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The term cardiovascular diseases (CVD) refers to disorders of heart and blood vessels, and include coronary heart disease, cerebrovascular disease, peripheral vascular disease, and heart failure, among others. Atherosclerosis is a common background of these diseases. It is not infrequent that some acute diseases, such as coronary syndromes, appear superimposed on a chronic arterial disease. Acute coronary syndromes (ACS), found worldwide among the leading causes of death, can be the origin of disabling chronic CVD such as heart failure [46]. Clinical and experimental evidence associates this group of alterations with an inflammatory process that takes part in its pathophysiology. In fact, inflammation is one of the most important factors for its initiation, progression, and consolidation [6].

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